Aberrant post‐translational modifications are a key molecular event that triggers the loss of p53 tumor suppressive function in tumors.[8] p53 is the first identified non‐histone protein with acetylation modification capacity,[9] and acetylation is a critical requisite for p53 activation.[10] In general, p53 acetylation is carried out by histone acetyltransferase (HATs), including p300/CBP/PCAF or Tip60/MOF/MOZ on multiple lysine residues. This evidence concerns the gene EP300 and neoplasm.